A myositis syndrome has been recognized for more than a decade in California sea lions (CSLs; Zalophus californianus) but a detailed description of the lesions and potential causes of this condition is lacking. The tissues of 136 stranded CSLs with rhabdomyositis were examined. Rhabdomyositis was considered incidental in 67% (91/136) of the CSLs, and a factor contributing to the animal stranding (significant rhabdomyositis) in 33% (45/136). Of the 91 cases with incidental rhabdomyositis, lesions consisted of a few small foci of lymphohistiocytic inflammation. Of the 45 cases with significant rhabdomyositis, 28 (62%) also presented with major comorbidities such as leptospirosis (2 animals) and domoic acid toxicosis (6 animals), whereas 17 (38%) had severe polyphasic rhabdomyositis as the only major disease process associated with mortality. In these animals, most striated muscles had multiple white streaks and diffuse atrophy. Microscopically, there was myofiber necrosis surrounded by lymphocytes and histiocytes admixed with areas of myofiber regeneration, and/or moderate to severe rhabdomyocyte atrophy usually adjacent to intact Sarcocystis neurona cysts. At the interface of affected and normal muscle, occasional T lymphocytes infiltrated the sarcoplasm of intact myocytes, and occasional myofibers expressed MHCII proteins in the sarcoplasm. S. neurona antibody titers and cyst burden were higher in animals with significant polymyositis antibody titers of (26125 ± 2164, 4.5 ± 1.2 cysts per section) and active myonecrosis than animals with incidental rhabdomyositis antibody titers of (7612 ± 1042, 1.7 ± 0.82 cysts per section). The presented findings suggest that S. neurona infection and immune-mediated mechanisms could be associated with significant polyphasic rhabdomyositis in CSLs.

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One of the greatest metabolic costs for endotherms is the energy allocated to thermoregulation. Weddell seals (Leptonychotes weddellii) are the southernmost breeding mammals, and as such are born into one of the most challenging thermal environments on the planet. During their nursing period, Weddell seal pups must develop the capability to survive both on the ice and in the water. Pups also concurrently shift from the use of fur to a reliance on blubber for insulation. This study examined the thermal and energetic costs associated with development and thermoregulation in Weddell seal pups. Metabolic rate (MR) in air was measured longitudinally for 4 pups every 2 weeks, starting at 1 week of age through the transition to independence (7 weeks); MR in water was measured in the same pups beginning at 3 weeks. Additionally, we assessed the molt status of each pup, and estimated body composition (blubber vs. lean mass) based on an elliptical cones model. There was a high degree of individual variability in mass‐specific MR in air in 1 week old pups (5.96–10.87 ml O2 min−1 kg−1), though in general it remained stable or decreased slightly from 1–7 weeks of age. Mass‐specific MR in water declined from 3 weeks to 7 weeks of age for 2 of the 4 pups, and remained stable for 2 pups. The difference between mass‐specific MR in air and in water also decreased from 3 to 7 weeks for 2 pups and remained steady for 2 pups; but by 5 weeks of age the difference between MR in air and in water was marginal for all 4 pups. Timing of the initiation of the molt and molt duration was also variable; two pups had molted patches by 3 weeks of age, and all but 1 pup were fully molted by 7 weeks of age. All pups gained mass from 1 to 5 weeks of age at an average rate of 2.02 ± 0.09 kg day−1 and the proportion of blubber increased from 1–3 weeks (25% to 38% of body mass). Blubber proportion remained steady from 3–5 weeks (38% to 40% of body mass) because pups gained proportionally more lean mass (61% of total mass gained). By 7 weeks, 3 of the 4 pups had weaned and were losing mass. Timing of MR equivalence in air and water did not vary with molt status (amount of lanugo) or with estimated body composition. Overall, these results indicate that Weddell seal pups have developed their thermal capabilities by ~5 weeks of age to protect themselves against increased heat loss in water, independent of the amount of lanugo fur or body composition.Support or Funding InformationThis project was funded by the National Science Foundation, Office of Polar Programs (#1543539).This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

OBJECTIVE To describe clinical signs, treatment, and outcome for California sea lions (Zalophus californianus) with Sarcocystis-associated polyphasic rhabdomyositis. ANIMALS 38 free-ranging juvenile to adult California sea lions examined at a rehabilitation center in California between September 2015 and December 2017. PROCEDURES Medical records at The Marine Mammal Center were reviewed to identify sea lions in which sarcocystosis had been diagnosed. RESULTS Clinical signs were highly variable and associated with polyphasic rhabdomyositis attributed to Sarcocystis neurona infection. Generalized severe muscle wasting, respiratory compromise, and regurgitation secondary to megaesophagus were the most profound clinical findings. Respiratory compromise and megaesophagus were associated with a poor prognosis. Eight of the 38 sea lions were treated and released to the wild, and 2 subsequently restranded and were euthanized. Two additional animals received no targeted treatment and were released. The remaining 28 animals were either euthanized or died during treatment. CONCLUSIONS AND CLINICAL RELEVANCE Results suggested that unlike other marine mammals, which typically develop encephalitis, California sea lions with sarcocystosis often have polyphasic rhabdomyositis with highly variable clinical signs and that extensive diagnostic testing may be required to confirm the diagnosis. Treatment with an antiprotozoal drug in combination with corticosteroids may resolve clinical disease, but the prognosis is guarded.